Key result
Telmisartan showed no differential treatment effect on cardiovascular outcomes between hypertensive and nonhypertensive patients, though it reduced the secondary composite endpoint in hypertensives (13.0% vs 15.0%, P<0.05).
Why the study?
Does telmisartan reduce cardiovascular events differentially in hypertensive versus nonhypertensive ACE-intolerant patients at high cardiovascular risk?
RCT
Does telmisartan reduce cardiovascular events differentially in hypertensive versus nonhypertensive ACE-intolerant patients at high cardiovascular risk?
In a post-hoc analysis of high-risk ACE-intolerant patients, telmisartan did not show a significantly differential effect on primary cardiovascular outcomes based on baseline hypertension status, though it may offer specific benefits like reduced MI and LVH in hypertensive patients.
No differential primary effect by hypertension status; leaves open secondary benefits in hypertensives as hypothesis-generating.
BACKGROUND: In the Telmisartan Randomised AssessmeNt Study in ACE iNtolerant subjects with cardiovascular Disease, all patients were at high cardiovascular risk, and a substantial proportion were hypertensive. We performed a post-hoc analysis to explore the hypothesis that telmisartan has a differential action in hypertensive vs. nonhypertensive patients. METHODS: The primary four-fold endpoint (composite of cardiovascular death, myocardial infarction (MI), stroke, or hospitalization for heart failure), the secondary three-fold endpoint (cardiovascular death, MI, and stroke), the individual components, new onset of left ventricular hypertrophy (LVH), and new onset of albuminuria were analyzed. RESULTS: There was no evidence for a significantly differential treatment effect of telmisartan in hypertensive and nonhypertensive patients for any endpoints, although the occurrence of the secondary three-fold endpoint was significantly lower in the telmisartan group (13.0%) compared with placebo (15.0%, P < 0.05) only in hypertensive patients. Moreover, data from this post-hoc analysis suggest that MI may be less frequent in hypertensive patients treated with telmisartan (3.8 vs. 5.1%; P < 0.05). Telmisartan may also reduce new onset of LVH (nonhypertensive patients P < 0.05; hypertensive patients P < 0.001) in both subgroups, and new onset of microalbuminuria and macroalbuminuria in hypertensive patients (P < 0.001 and P < 0.01, respectively).The effect of telmisartan in hypertensive and nonhypertensive patients at high cardiovascular risk was not different. This post-hoc analysis suggests that MI may be further reduced by telmisartan in hypertensive patients. Further investigations are needed to study the hypotheses raised by this explanatory analysis.
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Foulquier et al. (2014) conducted an RCT in ACE intolerant subjects with cardiovascular disease at high cardiovascular risk. Telmisartan vs. Placebo was evaluated on Composite of cardiovascular death, myocardial infarction (MI), stroke, or hospitalization for heart failure. Telmisartan showed no differential treatment effect on cardiovascular outcomes between hypertensive and nonhypertensive patients, though it reduced the secondary composite endpoint in hypertensives (13.0% vs 15.0%, P<0.05).
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